The overall objective of this project is to learn the cellular and metabolic basis for the altered lung mechanics and gas exchange in a model of chemical lung injury in which necrosis of both types of alveolar epithelial cells is the principal lesion. During previous studies of the chronic lung injury induced in the hamster by repeated small injections of N-nitroso-N-methyl urethane (NNNMU), we noted that single large doses cause rapidly fatal acute respiratory failure and that alveolar epithelial necrosis was prominent on electron microscopic examination of the lungs of these animals. The goal for the current year and the previous year has been to study the evolution of this acute lesion by light and electron microscopy and to test the hypothesis that epithelial necrosis is solely or principally responsible for the altered lung function in these animals.